The treatment of fibromyalgia can be difficult. Recommendations often include getting enough sleep, exercising regularly, and eating a healthy diet.[4] Cognitive behavioral therapy may also be helpful.[3] The medications duloxetine, milnacipran, or pregabalin may be used.[4] Use of opioid pain medication is controversial with some stating their use is poorly supported by evidence[4][7] and others saying that weak opioids may be reasonable if other medications are not effective.[8] Dietary supplements also lack evidence to support their use. While fibromyalgia can last a long time, it does not result in death or tissue damage.[4]

Fibromyalgia is estimated to affect 2–8% of the population. Females are affected about twice as often as males. Rates appear similar in different areas of the world and among different cultures. Fibromyalgia was first defined in 1990 with updated criteria in 2011.[3] There is controversy about the classification, diagnosis, and treatment of fibromyalgia.[9][10] While some feel the diagnosis of fibromyalgia may negatively affect a person, other research finds it to be beneficial.[3] The term "fibromyalgia" is from New Latin, fibro-, meaning "fibrous tissues", Greek μυώ myo-, "muscle", and Greek άλγος algos, "pain"; thus the term literally means "muscle and fibrous connective tissue pain".[11]

Classification

Fibromyalgia is classed as a disorder of pain processing due to abnormalities in how pain signals are processed in the central nervous system.[12] The American College of Rheumatology classify fibromyalgia as being a functional somatic syndrome.[9] The expert committee of the European League Against Rheumatism classify fibromyalgia as a neurobiological disorder and as a result exclusively give pharmacotherapy their highest level of support.[9] The International Classification of Diseases (ICD-10) lists fibromyalgia as a diagnosable disease under "Diseases of the musculoskeletal system and connective tissue," under the code M79-7, and states that fibromyalgia syndrome should be classified as a functional somatic syndrome rather than a mental disorder. Although mental disorders and some physical disorders commonly are co-morbid with fibromyalgia – especially anxiety, depression, irritable bowel syndrome, and chronic fatigue syndrome – the ICD states that these should be diagnosed separately.[9]

Differences in psychological and autonomic nervous system profiles among affected individuals may indicate the existence of fibromyalgia subtypes. A 2007 review divides individuals with fibromyalgia into four groups as well as "mixed types":[13]

"extreme sensitivity to pain but no associated psychiatric conditions" (may respond to medications that block the 5-HT3 receptor)

Cause

The cause of fibromyalgia is unknown. However, several hypotheses have been developed including "central sensitization".[14] This theory proposes that people with fibromyalgia have a lower threshold for pain because of increased reactivity of pain-sensitive nerve cells in the spinal cord or brain.[2] Neuropathic pain and major depressive disorder often co-occur with fibromyalgia – the reason for this comorbidity appears to be due to shared genetic abnormalities, which leads to impairments in monoaminergic, glutamatergic, neurotrophic, opioid and proinflammatory cytokine signaling. In these vulnerable individuals, psychological stress or illness can cause abnormalities in inflammatory and stress pathways which regulate mood and pain. Eventually, a sensitization and kindling effect occur in certain neurons leading to the establishment of fibromyalgia and sometimes a mood disorder.[22] The evidence suggests that the pain in fibromyalgia results primarily from pain processing pathways functioning abnormally. In simple terms, it can be described as the volume of the neurons being set too high and this hyper-excitability of pain processing pathways and under-activity of inhibitory pain pathways in the brain results in the affected individual experiencing pain. Some neurochemical abnormalities that occur in fibromyalgia also regulate mood, sleep, and energy, thus explaining why mood, sleep, and fatigue problems are commonly co-morbid with fibromyalgia.[12]

Lifestyle

Stress may be an important precipitating factor in the development of fibromyalgia.[30] Fibromyalgia is frequently comorbid with stress-related disorders such as chronic fatigue syndrome, posttraumatic stress disorder, irritable bowel syndrome and depression.[31] A systematic review found significant association between fibromyalgia and physical and sexual abuse in both childhood and adulthood, although the quality of studies was poor.[32] Poor lifestyles including being a smoker, obesity and lack of physical activity may increase the risk of an individual developing fibromyalgia.[33]

Two studies that employed single-voxel magnetic resonance spectroscopy (1H-MRS) reported metabolic abnormalities within the hippocampal complex in people with fibromyalgia. As the hippocampus plays crucial roles in maintenance of cognitive functions, sleep regulation, and pain perception, it was suggested that metabolic dysfunction of the hippocampus may be implicated in the appearance of these symptoms.[34][35]

Some authors have proposed that, because exposure to stressful conditions can alter the function of the hypothalamic-pituitary-adrenal (HPA) axis, the development of fibromyalgia may stem from stress-induced disruption of the HPA axis.[36]

Sleep disturbances

In 1975, Moldofsky and colleagues reported the presence of anomalous alpha wave activity (typically associated with arousal states) measured by electroencephalogram (EEG) during non-rapid eye movement sleep of "fibrositis syndrome".[17] By disrupting stage IV sleep consistently in young, healthy subjects, the researchers reproduced a significant increase in muscle tenderness similar to that experienced in "neurasthenic musculoskeletal pain syndrome" but which resolved when the subjects were able to resume their normal sleep patterns.[37]

Psychological factors

There is strong evidence that major depression is associated with fibromyalgia (1999),[38] although the nature of the association is debated.[39] A comprehensive review into the relationship between fibromyalgia and major depressive disorder (MDD) found substantial similarities in neuroendocrine abnormalities, psychological characteristics, physical symptoms and treatments between fibromyalgia and MDD, but currently available findings do not support the assumption that MDD and fibromyalgia refer to the same underlying construct or can be seen as subsidiaries of one disease concept.[40] Indeed, the sensation of pain has at least two dimensions: a sensory dimension which processes the magnitude and location of the pain, and an affective-motivational dimension which processes the unpleasantness. Accordingly, a study that employed functional magnetic resonance imaging to evaluate brain responses to experimental pain among people with fibromyalgia found that depressive symptoms were associated with the magnitude of clinically induced pain response specifically in areas of the brain that participate in affective pain processing, but not in areas involved in sensory processing which indicates that the amplification of the sensory dimension of pain in fibromyalgia occurs independently of mood or emotional processes.[41] Fibromyalgia has also been linked with bipolar disorder, particularly the hypomania component.[42]

Non-celiac gluten sensitivity

Pathophysiology

The brains of people with fibromyalgia show functional and structural differences from those of people without fibromyalgia, but it is unclear whether the brain anomalies cause fibromyalgia symptoms, or are the product of an unknown underlying common cause. Some research suggests that these brain anomalies may be the result of childhood stress, or prolonged or severe stress.[31]

Dopamine dysfunction

The "dopamine hypothesis of fibromyalgia" proposes that the central abnormality responsible for symptoms associated with fibromyalgia is a disruption of normal dopamine-related neurotransmission.[45] Insufficient dopamine in a part of the body is termed hypodopaminergia. Dopamine is a catecholamineneurotransmitter with roles in pain perception and natural analgesia. There is also strong evidence for a role of dopamine in restless leg syndrome,[46] which is a condition found frequently in people with fibromyalgia.[47] Some people with fibromyalgia responded to pramipexole, a dopamine agonist that selectively stimulates dopamine D2/D3 receptors and is used to treat both Parkinson's disease and restless leg syndrome.[48]

Decreased CSF levels of dopamine were reported in 1992, which may explain the efficacy of some dopaminergic agents in fibromyalgia.[49]

Poly-modal sensitivity

Results from studies examining responses to experimental stimulation suggest that people with fibromyalgia may have heightened sensitivity of the nociceptive system, which senses pressure, heat, cold, electrical and chemical stimulation.[56] Experiments examining pain regulatory systems have shown that people with fibromyalgia display an exaggerated wind-up in response to repetitive stimulation[57] and an absence of exercise-induced analgesic response.[58]

Neuroendocrine disruption

Levels of hormones under the direct or indirect control of growth hormone (GH), including insulin-like growth factor 1 (IGF-1), cortisol, leptin and neuropeptide Y may be abnormal in people with fibromyalgia.[59][60] Several authors have demonstrated low growth hormone levels or low IGF-I levels in patients with fibromyalgia compared with controls. Moreover, people with fibromyalgia have an abnormal sleep pattern involving stages 3 and 4 of non-REM sleep during which growth hormone is predominantly secreted.[61] Further support for a causal role for growth hormone deficiency comes from observations that such deficiency in adults has been associated with many of the symptoms described by people with fibromyalgia. Growth hormone is important in maintaining muscle homeostasis, and it has been suggested that low levels may be responsible for delayed healing of muscle microtrauma in fibromyalgia.[62] Low (IGF-1) levels in some people with fibromyalgia have led to the theory that these people may actually have a different, treatable syndrome, adult growth hormone deficiency.[63] However, there remains some disagreement about the role of HGH in fibromyalgia.[64]

People with fibromyalgia may have alterations of normal neuroendocrine function, characterized by mild hypocortisolemia,[65] hyperreactivity of pituitary adrenocorticotropin hormone release in response to challenge, and glucocorticoid feedback resistance.[66]

Other abnormalities include reduced responsivity of thyrotropin and thyroid hormones to thyroid-releasing hormone,[67] a mild elevation of prolactin levels with disinhibition of prolactin release in response to challenge[68] and hyposecretion of adrenal androgens.[69]

These changes might result from chronic stress, which, after being perceived and processed by the central nervous system, activates hypothalamic corticotrophin-releasing hormone neurons. Chronic overactivity of these neurons could disrupt normal function of the pituitary-adrenal axis and cause an increased stimulation of hypothalamic somatostatin secretion, which, in turn, could inhibit the secretion of other hormones.[70]

Sympathetic hyperactivity

Functional analysis of the autonomic system in people with fibromyalgia has demonstrated disturbed activity characterized by hyperactivity of the sympathetic nervous system at baseline[71] with reduced sympathoadrenal reactivity in response to a variety of stressors including physical exertion and mental stress.[72][73] People with fibromyalgia demonstrate lower heart rate variability, an index of sympathetic/parasympathetic balance, indicating sustained sympathetic hyperactivity, especially at night.[74] In addition, plasma levels of neuropeptide Y, which is co-localized with norepinephrine in the sympathetic nervous system, have been reported as low in people with fibromyalgia,[60] while circulating levels of epinephrine and norepinephrine have been variously reported as low, normal and high.[75][76] Administration of interleukin-6, a cytokine capable of stimulating the release of hypothalamic corticotropin-releasing hormone which in turn stimulates activity within the sympathetic nervous system, results in a dramatic increase in circulating norepinephrine levels and a significantly greater increase in heart rate over baseline in people with fibromyalgia as compared to healthy controls.[77]

Brain imaging studies

Evidence of abnormal brain involvement in fibromyalgia has been provided via functional neuroimaging. The first findings reported were decreased blood flow within the thalamus and elements of the basal ganglia and mid-brain (i.e., pontine nucleus).[83][84] Differential activation in response to painful stimulation has also been demonstrated.[85][86] Brain centers showing hyperactivation in response to noxious stimulation include such pain-related brain centers as the primary and secondary somatosensory cortices, anterior cingulate cortex, and insular cortex. People also exhibit neural activation in brain regions associated with pain perception in response to nonpainful stimuli in such areas as the prefrontal, supplemental motor, insular, and cingulate cortices.

Evidence of hippocampal disruption indicated by reduced brain metabolite ratios has been demonstrated by studies using single-voxel magnetic resonance spectroscopy (1H-MRS).[34][35] A significant negative correlation was demonstrated between abnormal metabolite ratios and a validated index of the clinical severity (i.e. the Fibromyalgia Impact Questionnaire).[87] Correlations between clinical pain severity and concentrations of the excitatory amino acid neurotransmitter glutamate within the insular cortex have also been demonstrated using 1H-MRS.[88]

An acceleration of normal age-related brain atrophy has been demonstrated using voxel-based morphometry (VBM) with areas of reduced gray matter located in the cingulate cortex, insula and parahippocampal gyrus. Grey matter loss appears to increase 9.5 times the normal rate with each year.[89] Studies utilizing positron emission tomography have demonstrated reduced dopamine synthesis in the brainstem and elements of the limbic cortex.[90]

A significant negative correlation between pain severity and dopamine synthesis was demonstrated within the insular cortex. A subsequent study demonstrated gross disruption of dopaminergic reactivity in response to a tonic pain stimulus within the basal ganglia with a significant positive correlation between the defining feature of the disorder (i.e. tender point index) and dopamine D2 receptor binding potential specifically in the right putamen.[91]

Finally, reduced availability of mu-opioid receptors in the ventral striatum/nucleus accumbens and cingulate cortex has been demonstrated, with a significant negative correlation between affective pain levels and receptor availability in the nucleus accumbens.[92]

People with FMS consistently demonstrate altered activity in the insula, amygdala, anterior/mid cingulate cortex, superior temporal gyrus, the primary and secondary somatosensory cortex, and lingual gyrus. The changes show similarities to those found in other chronic pain conditions, but it is not known whether these specific features relate to all chronic pain or just to FMS.[93]

Diagnosis

There is no single test that can fully diagnose fibromyalgia and there is debate over what should be considered essential diagnostic criteria and whether an objective diagnosis is possible. In most cases, people with fibromyalgia symptoms may also have laboratory test results that appear normal and many of their symptoms may mimic those of other rheumatic conditions such as arthritis or osteoporosis. The most widely accepted set of classification criteria for research purposes was elaborated in 1990 by the Multicenter Criteria Committee of the American College of Rheumatology. These criteria, which are known informally as "the ACR 1990", define fibromyalgia according to the presence of the following criteria:

A history of widespread pain lasting more than three months – affecting all four quadrants of the body, i.e., both sides, and above and below the waist.

Tender points – there are 18 designated possible tender points (although a person with the disorder may feel pain in other areas as well). Diagnosis is no longer based on the number of tender points.[94][95]

The ACR criteria for the classification of patients were originally established as inclusion criteria for research purposes and were not intended for clinical diagnosis but have now become the de facto diagnostic criteria in the clinical setting. It should be noted that the number of tender points that may be active at any one time may vary with time and circumstance. A controversial study was done by a legal team looking to prove their client's disability based primarily on tender points and their widespread presence in non-litigious communities prompted the lead author of the ACR criteria to question now the useful validity of tender points in diagnosis.[96] Use of control points has been used to cast doubt on whether a person has fibromyalgia, and to claim the person is malingering; however, no research has been done for the use of control points to diagnose fibromyalgia, and such diagnostic tests have been advised against, and people complaining of pain all over should still have fibromyalgia considered as a diagnosis.[9]

2010 provisional criteria

Widespread Pain Index (WPI) Areas

In 2010, the American College of Rheumatology approved provisional revised diagnostic criteria for fibromyalgia that eliminated the 1990 criteria's reliance on tender point testing.[97] The revised criteria use a widespread pain index (WPI) and symptom severity scale (SS) in place of tender point testing under the 1990 criteria. The WPI counts up to 19 general body areas[lower-alpha 1] in which the person has experienced pain in the preceding two weeks. The SS rates the severity of the person's fatigue, unrefreshed waking, cognitive symptoms, and general somatic symptoms,[lower-alpha 2] each on a scale from 0 to 3, for a composite score ranging from 0 to 12. The revised criteria for diagnosis are:

WPI ≥ 7 and SS ≥ 5 OR WPI 3–6 and SS ≥ 9,

Symptoms have been present at a similar level for at least three months, and

Differential diagnosis

Two patients initially diagnosed with fibromyalgia were subsequently shown to have myotonia congenita.[98] Both patients had been seen by rheumatologists and diagnosed with fibromyalgia. The diagnoses were revised when electromyographic studies revealed myotonic discharges in some of the muscles. Genetic analysis of the skeletal muscle chloride channel which is the underlying cause of myotonia congenita revealed that both patients had mutations in this gene. Over 130 mutations in this gene have been described and the phenotype is very variable which may account for the difficulty in the initial diagnosis.[99][100]

Management

As with many other medically unexplained syndromes, there is no universally accepted treatment or cure for fibromyalgia, and treatment typically consists of symptom management. Developments in the understanding of the pathophysiology of the disorder have led to improvements in treatment, which include prescription medication, behavioral intervention, and exercise. Indeed, integrated treatment plans that incorporate medication, patient education, aerobic exercise and cognitive behavioral therapy have been shown to be effective in alleviating pain and other fibromyalgia-related symptoms.[101]

Antidepressants

Antidepressants are "associated with improvements in pain, depression, fatigue, sleep disturbances, and health-related quality of life in people with FMS."[107] The goal of antidepressants should be symptom reduction and if used long term, their effects should be evaluated against side effects. A small number of people benefit significantly from the SNRIs duloxetine and milnacipran and the tricyclic antidepressants (TCAs), such as amitriptyline. However many people experience more adverse effects than benefits.[108][109] While amitriptyline has been used as a first line treatment, the quality of evidence to support this use is poor.[110]

It can take up to three months to derive benefit from the antidepressant amitriptyline and up to six months to gain the maximal response from duloxetine, milnacipran, and pregabalin. Some medications have the potential to cause withdrawal symptoms when stopping so gradual discontinuation may be warranted particularly for antidepressants and pregabalin.[9]

Anti-seizure medication

The anti-convulsant drugs gabapentin[112] and pregabalin can be used to reduce pain.[113] Gabapentin is of a significant benefit in about 30% of people who take it. However, it is commonly associated with adverse effects.[112] Pregabalin demonstrates a substantial benefit in about 9% of people.[114] Pregabalin reduced time off work by 0.2 days per week.[115]

Opioids

The use of opioids is controversial. As of 2015 no opioid is approved for use in this condition by the FDA.[116] The National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) in 2014 stated that there was a lack of evidence for opioids.[4] The Association of the Scientific Medical Societies in Germany in 2012 made no recommendation either for or against the use of weak opioids because of the limited amount of scientific research addressing their use in the treatment of FM. They strongly advise against using strong opioids.[102] The Canadian Pain Society in 2012 said that opioids, starting with a weak opioid like tramadol, can be tried but only for people with moderate to severe pain that is not well-controlled by non-opioid painkillers. They discourage the use of strong opioids and only recommend using them while they continue to provide improved pain and functioning. Healthcare providers should monitor people on opioids for ongoing effectiveness, side effects and possible unwanted drug behaviors.[104]

The European League Against Rheumatism in 2008 recommends tramadol and other weak opioids may be used for pain but not strong opioids.[103] A 2015 review found fair evidence to support tramadol use if other medications do not work.[116] Goldenberg et al suggest that tramadol works via its serotonin and norepinephrine reuptake inhibition, rather than via its action as a weak opioid receptor agonist.[7] The combination of tramadol and paracetemol has demonstrated efficacy, safety and tolerability (for up to two years in the management of other pain conditions) without the development of tolerance. It is as effective as a combination of codeine (another mild opioid) and paracetamol but produces less sleepiness and constipation.[117]

A large study of US people with fibromyalgia found that between 2005 and 2007 37.4% were prescribed short-acting opioids and 8.3% were prescribed long-acting opioids,[118] with around 10% of those prescribed short-acting opioids using tramadol;[119] and a 2011 Canadian study of 457 people with FM found 32% used opioids and two thirds of those used strong opioids.[104]

Others

A 2007 review of three randomized placebo controlled studies concluded that a period of nine months of growth hormone was required to reduce fibromyalgia symptoms and normalize IGF-1.[120] A 2014 also found some evidence support its use.[121]Sodium oxybate increases growth hormone production levels through increased slow-wave sleep patterns. However, this medication was not approved by the FDA for the indication for use in people with fibromyalgia due to the concern for abuse.[122]

Dopamine agonists (e.g. pramipexole and ropinirole) resulted in some improvement in a minority of people,[48] but numerous side effects, including the onset of impulse control disorders like compulsive gambling and shopping, have led to concern about this approach.[125]

Therapy

Due to the uncertainty about the pathogenesis of FM, current treatment approaches focus on management of symptoms to improve quality of life,[128] using integrated pharmacological and non-pharmacological approaches.[129] There is no single intervention shown to be effective for all patients [130] and no gold treatment standard exists for FM.[131] Multimodal/multidisciplinary therapy is recommended to target multiple underlying factors of FM.[132] A meta-analysis of 1,119 subjects found "strong evidence that multicomponent treatment has beneficial short-term effects on key symptoms of FMS." [133]

Cognitive behavioural therapy

Non-pharmacological components include cognitive-behavioural therapy (CBT), exercise and psychoeducation (specifically, sleep hygiene).[134][135][136][137] CBT and related psychological and behavioural therapies have a small to moderate effect in reducing symptoms of fibromyalgia.[138][139] Effect sizes tend to be small when CBT is used as a stand-alone treatment for FM patients, but these improve significantly when CBT is part of a wider multidisciplinary treatment program.[140] The greatest benefit occurs when CBT is used along with exercise.[101][141]

A 2010 systematic review of 14 studies reported that CBT improves self-efficacy or coping with pain and reduces the number of physician visits at post-treatment, but has no significant effect on pain, fatigue, sleep or health-related quality of life at post-treatment or follow-up. Depressed mood was also improved but this could not be distinguished from some risks of bias.[142]

Exercise

Exercise improves fitness and sleep and may reduce pain and fatigue in some people with fibromyalgia.[143][144] In particular, there is strong evidence that cardiovascular exercise is effective for some people.[145] Long-term aquatic-based exercise has been proven beneficial as it combines cardiovascular exercise with resistance training.[146]

In children, fibromyalgia is often treated with an intense physical and occupational therapy program for amplified musculoskeletal pain syndromes. These programs also employ counseling, art therapy, and music therapy. These programs are evidence-based and report long-term total pain resolution rates as high as 88%.[147]

Prognosis

Although in itself neither degenerative nor fatal, the chronic pain of fibromyalgia is pervasive and persistent. Most people with fibromyalgia report that their symptoms do not improve over time. An evaluation of 332 consecutive new people with fibromyalgia found that disease-related factors such as pain and psychological factors such as work status, helplessness, education, and coping ability had an independent and significant relationship to FM symptom severity and function.[148]

Epidemiology

Fibromyalgia is estimated to affect 2–8% of the population,[3][149] with a female to male incidence ratio that is somewhere between 7:1 and 9:1.[14][150]

Fibromyalgia may not be diagnosed in up to 75% of affected people.[12]

History

Chronic widespread pain had already been described in the literature in the 19th century but the term fibromyalgia was not used until 1976 when Dr P.K. Hench used it to describe these symptoms.[9] Many names, including "muscular rheumatism", "fibrositis", "psychogenic rheumatism", and "neurasthenia" were applied historically to symptoms resembling those of fibromyalgia.[151] The term fibromyalgia was coined by researcher Mohammed Yunus as a synonym for fibrositis and was first used in a scientific publication in 1981.[152] Fibromyalgia is from the Latinfibra (fiber)[153] and the Greek words myo (muscle)[154] and algos (pain).[155]

Historical perspectives on the development of the fibromyalgia concept note the "central importance" of a 1977 paper by Smythe and Moldofsky on fibrositis.[156][157] The first clinical, controlled study of the characteristics of fibromyalgia syndrome was published in 1981,[158] providing support for symptom associations. In 1984, an interconnection between fibromyalgia syndrome and other similar conditions was proposed,[159] and in 1986, trials of the first proposed medications for fibromyalgia were published.[159]

Society and culture

Economics

People with fibromyalgia generally have higher health care costs and utilization rates. A study of almost 20,000 Humana members enrolled in Medicare Advantage and commercial plans compared costs and medical utilizations and found that people with fibromyalgia used twice as much pain-related medication as those without fibromyalgia. Furthermore, the use of medications and medical necessities increased markedly across many measures once diagnosis was made.[162]

Controversies

Being a disorder defined relatively recently and still not completely understood, fibromyalgia continues to be a diagnosis that sometimes is disputed. Dr. Frederick Wolfe, lead author of the 1990 paper that first defined the diagnostic guidelines for fibromyalgia, stated in 2008, that he believed it "clearly" not to be a disease but instead a physical response to depression and stress,[163] and in 2013 that its causes "are controversial in a sense" and "there are many factors that produce these symptoms – some are psychological and some are physical and it does exist on a continuum".[164]

Some members of the medical community do not consider fibromyalgia a disease because of a lack of abnormalities on physical examination and the absence of objective diagnostic tests.[156][165] Yunus objects to the psychological characterization of FM. He argues that data indicating it is not psychological has been ignored or manipulated.[166]

Neurologists and pain specialists tend to view fibromyalgia as a pathology due to dysfunction of muscles and connective tissue as well as functional abnormalities in the central nervous system. Rheumatologists define the syndrome in the context of "central sensitization" – heightened brain response to normal stimuli in the absence of disorders of the muscles, joints, or connective tissues. On the other hand, psychiatrists often view fibromyalgia as a type of affective disorder, whereas specialists in psychosomatic medicine tend to view fibromyalgia as being a somatic symptom disorder. However, there is extensive research evidence to support the view that the central symptom of fibromyalgia, namely pain, has a neurogenic origin. These controversies don't engage healthcare specialists alone; some patients object to fibromyalgia being described in purely somatic terms.[9][12]

The validity of fibromyalgia as a unique clinical entity is a matter of contention because "no discrete boundary separates syndromes such as FMS, chronic fatigue syndrome, irritable bowel syndrome, or chronic muscular headaches".[145][167] Because of this symptomatic overlap, some researchers have proposed that fibromyalgia and other analogous syndromes be classified together as functional somatic syndromes for some purposes.[168]